HYPERVENTILATION: ANALYSIS OF CLINICAL SYMPTOMATOLOGY

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Abstract
Hyperventilation may occur as a response to certain intense emotional experiences in normal people, as a vegetative neurotic symptom, as an hysterical symptom, as a symptom of diffuse encephalopathy and certain drugs, and as a response to anoxia. The symptoms may be divided into those related to reduction in consciousness and those related to tetany. Reduction in consciousness is found to correlate well with the degree of slowing of the electroencephalogram and is usually marked when the mean frequency is reduced below 5.0/sec. Slowing of E.E.G. frequency during hyperventilation is more marked with: rapid reduction in arterial CO2 content; low blood sugar; low oxygen tension of inspired air; the erect posture; and amyl nitrite and nitroglycerine. Conversely, high blood sugar, high O2 tension, and the recumbent posture diminish E.E.G. slowly. Intraven. injn. of CaCl2 and nicotinic acid has no effect on E.E.G. during hyperventilation. Tetany is unrelated to changes in E.E.G. and occurs with longer periods of hyperventilation. The numbness and tingling probably are also peripheral in origin. Actual syncope is unusual during hyperventilation. Four different mechanisms have been observed: concurrent or delayed vasodepressor syncope; accentuation of already present orthostatic hypotension; hysterical syncope; and central type.